Poor ovarian reserve is a condition of low fertility characterized by 1): low numbers of remaining oocytes in the ovaries or 2) possibly impaired preantral oocyte development or recruitment. Recent research suggests that premature ovarian aging and premature ovarian failure (aka primary ovarian insufficiency) may represent a continuum of premature ovarian senescence. It is usually accompanied by high FSH (follicle stimulating hormone) levels.

Quality of the eggs (oocytes) may also be impaired as a 1989 study by Scott et al. of 758 in vitro fertilisation (IVF) cycles showed a dramatic decline in implantation rates between high (> 25 mIU/mL) and low day three FSH (<15 mIU/mL) women even though the ages of the women were equivalent between the two groups (mean age 35 years). However, other studies show no association with elevated FSH levels and genetic quality of embryos after adjusting for age. The decline in quality was age related, not FSH related as the younger women with high day three FSH levels had higher live birth rates than the older women with high FSH. There was no significant difference in genetic embryo quality between same aged women regardless of FSH levels. A 2008 study concluded that diminished reserve did not affect the quality of oocytes and any reduction in quality in diminished reserve women was age related. One expert concluded: in young women with poor reserve when eggs are obtained they have near normal rates of implantation and pregnancy rates, but they are at high risk for IVF cancellation; if eggs are obtained, pregnancy rates are typically better than in older woman with normal reserve. However, if the FSH level is extremely elevated these conclusions are likely not applicable.

On average, the ovaries supply a woman with eggs until age 51, the average age of natural menopause.

POF is not the same as a natural menopause, in that the dysfunction of the ovaries, loss of eggs, or removal of the ovaries at a young age is not a normal physiological occurrence.

Infertility is the result of this condition, and is the most discussed problem resulting from it, but there are additional health implications of the problem, and studies are ongoing. For example, osteoporosis or decreased bone density affects almost all women with POF due to an insufficiency of estrogen. There is also an increased risk of heart disease, hypothyroidism in the form of Hashimoto's thyroiditis, Addison's disease, and other auto-immune disorders.

Hormonally, POF is defined by abnormally low levels of estrogen and high levels of FSH, which demonstrate that the ovaries are no longer responding to circulating FSH by producing estrogen and developing fertile eggs. The ovaries will likely appear shriveled.

The age of onset can be as early as the teenage years, or can even exist from birth, but varies widely. If a girl never begins menstruation, it is called primary ovarian failure. The age of 40 was chosen as the cut-off point for a diagnosis of POF. This age was chosen somewhat arbitrarily, as all women's ovaries decline in function over time. However an age needed to be chosen to distinguish usual menopause from the abnormal state of premature menopause. Premature ovarian failure has components to it that distinguish it from normal menopause.

By the age of 40, approximately one percent of women have POF. Women suffering from POF usually experience menopausal symptoms that are more severe than the symptoms found in older menopausal women.

The most common words women use to describe how they felt in the 2 hours after being given the diagnosis of primary ovarian insufficiency are "devastated, "shocked," and "confused." These are words that describe emotional trauma. The diagnosis is more than infertility and affects a woman’s physical and emotional well-being. Patients face the acute shock of the diagnosis, associated stigma of infertility, grief from the death of dreams, anxiety and depression from the disruption of life plans, confusion around the cause, symptoms of estrogen deficiency, worry over the associated potential medical sequelae such as reduced bone density and cardiovascular risk, and the uncertain future that all of these factors create. There is a need for an evidence-based integrative medicine program to assist women with primary ovarian insufficiency. Presently such a program does not exist in the community, but a community of practice has formed to address this deficiency. Women with primary ovarian insufficiency perceive lower social support than control women, so building a trusted community of practice for them would be expected to improve their well being. It is important to connect women with primary ovarian insufficiency to an appropriate collaborative care team because the condition has been clearly associated with suicide related to the stigma of infertility. Suicide rates are known to be increased in women who experience infertility.

Amenorrhoea is the absence of a menstrual period in a woman of reproductive age. Physiological states of amenorrhoea are seen, most commonly, during pregnancy and lactation (breastfeeding), the latter also forming the basis of a form of contraception known as the lactational amenorrhoea method. Outside the reproductive years, there is absence of menses during childhood and after menopause.

Amenorrhoea is a symptom with many potential causes.

Primary amenorrhoea (menstrual cycles never starting) may be caused by developmental problems, such as the congenital absence of the uterus or failure of the ovary to receive or maintain egg cells. Also, delay in pubertal development will lead to primary amenorrhoea. It is defined as an absence of secondary sexual characteristics by age 14 with no menarche or normal secondary sexual characteristics but no menarche by 16 years of age.

Secondary amenorrhoea (menstrual cycles ceasing) is often caused by hormonal disturbances from the hypothalamus and the pituitary gland, from premature menopause or intrauterine scar formation. It is defined as the absence of menses for three months in a woman with previously normal menstruation or nine months for women with a history of oligomenorrhoea.

Children who are healthy but have a slower rate of physical development than average have constitutional delay of growth and puberty. These children have a history of stature shorter than their age-matched peers throughout childhood, but their height is appropriate for bone age, and skeletal development is delayed more than 2.5 SD. They usually are thin and often have a family history of delayed puberty. Children with a combination of a family tendency toward short stature and constitutional delay of growth and puberty are the most likely to seek evaluation. They quite often seek evaluation when classmates or friends undergo pubertal development and growth, thereby accentuating their delay.

It is often difficult to establish if it is a true constitutional delay of growth and puberty or if there is an underlying pathology, because biochemical tests are not always discriminatory. Short stature, delayed growth in height and weight, and/or delayed puberty may be the only clinical manifestations of coeliac disease, in absence of any other symptoms.

There are two primary ways to classify amenorrhoea. Types of amenorrhoea are classified as primary or secondary, or based on functional "compartments". The latter classification relates to the hormonal state of the patient that hypo-, eu-, or hypergonadotropic (whereby interruption to the communication between gonads and follicle stimulating hormone (FSH) causes FSH levels to be either low, normal or high).

- By primary vs. secondary: Primary amenorrhoea is the absence of menstruation in a woman by the age of 16. As pubertal changes precede the first period, or menarche, female children by the age of 14 who still have not reached menarche, plus having no sign of secondary sexual characteristics, such as thelarche or pubarche—thus are without evidence of initiation of puberty—are also considered as having primary amenorrhoea. Secondary amenorrhoea is where an established menstruation has ceased—for three months in a woman with a history of regular cyclic bleeding, or nine months in a woman with a history of irregular periods. This usually happens to women aged 40–55. However, adolescent athletes are more likely to experience disturbances to the menstrual cycle than athletes of any other age. Amenorrhoea may cause serious pain in the back near the pelvis and spine. This pain has no cure, but can be relieved by a short course of progesterone to trigger menstrual bleeding.

- By compartment: The reproductive axis can be viewed as having four compartments: 1. outflow tract (uterus, cervix, vagina), 2. ovaries, 3. pituitary gland, and 4. hypothalamus. Pituitary and hypothalamic causes are often grouped together.

There is some controversy as the accuracy of the tests used to predict poor ovarian reserve. One systematic review concluded that the accuracy of predicting the occurrence of pregnancy is very limited. When a high threshold is used, to prevent couples from wrongly being refused IVF, only approximately 3% of IVF-indicated cases are identified as having unfavourable prospects in an IVF treatment cycle. Also, the review concluded the use of any ORT (Ovarian Reserve Testing) for outcome prediction cannot be supported. Also Centers for Disease Control and Prevention statistics show that the success rates for IVF with diminished ovarian reserve vary widely between IVF centers.

Studies indicate that breast development in girls and the appearance of pubic hair in girls and boys are starting earlier than in previous generations. As a result, "early puberty" in children, particularly girls, as young as 9 and 10 is no longer considered abnormal, although it may be upsetting to parents and can be harmful to children who mature physically at a time when they are immature mentally.

No age reliably separates normal from abnormal processes in children, but the following age thresholds for evaluation are thought to minimize the risk of missing a significant medical problem:

- Breast development in boys before appearance of pubic hair or testicular enlargement,

- Pubic hair or genital enlargement (gonadarche) in boys with onset before 9.5 years,

- Pubic hair (pubarche) before 8 or breast development (thelarche) in girls with onset before 7 years,

- Menstruation (menarche) in girls before 10 years.

Medical evaluation is sometimes necessary to recognize the few children with serious conditions from the majority who have entered puberty early but are still medically normal. Early sexual development warrants evaluation because it may:

- induce early bone maturation and reduce eventual adult height,

- indicate the presence of a tumour or other serious problem,

- cause the child, particularly a girl, to become an object of adult sexual interest.

If the cause can be traced to the hypothalamus or pituitary, the cause is considered central. Other names for this type are "complete" or "true precocious" puberty.

Causes of central precocious puberty can include:

- damage to the inhibitory system of the brain (due to infection, trauma, or irradiation),

- hypothalamic hamartoma produces pulsatile gonadotropin-releasing hormone (GnRH),

- Langerhans cell histiocytosis, or

- McCune–Albright syndrome.

Central precocious puberty can be caused by intracranial neoplasm, infection (most commonly central nervous system tuberculosis especially in developing countries), trauma, hydrocephalus, and Angelman syndrome. Precocious puberty is associated with advancement in bone age, which leads to early fusion of epiphyses, thus resulting in reduced final height and short stature.

Precocious puberty can make a child fertile when very young, with the youngest mother on record being Lina Medina, who gave birth at the age of 5 years, 7 months and 17 days, in one report and at 6 years 5 months in another.

"Central precocious puberty (CPP) was reported in some patients with suprasellar arachnoid cysts (SAC), and SCFE (slipped capital femoral epiphysis) occurs in patients with CPP because of rapid growth and changes of growth hormone secretion."

If no cause can be identified, it is considered idiopathic or constitutional.

Premature thelarche is a rare medical condition that is characterized by isolated breast development (thelarche being the onset of breast development) at a very early age with no other signs of sexual maturation. It generally occurs within the first 1 to 4 years of life, with a peak incidence of 2 years of age, and tends to resolve within 1 to 2 years without treatment. The condition never advances beyond Tanner stage III breast development.

Premature thelarche is distinct from neonatal breast hyperplasia (see also witch's milk), which is common in the first few months of life and is due to acute exposure to high levels of sex hormones like estrogen during pregnancy. Premature thelarche is also distinct from precocious puberty, which generally occurs later in childhood and also includes development of other pubertal characteristics.

Treatment with fennel ("Foeniculum vulgare") has been associated with premature thelarche in several case reports. Estradiol levels were found to be elevated by 15–20 times for the ages of the afflicted girls (5 months to 5 years). Also, fennel is known to contain anethole, an estrogenic compound.

Approximate mean ages for the onset of various pubertal changes are as follows. Ages in parentheses are the approximate 3rd and 97th percentiles for attainment. For example, less than 3% of girls have not yet achieved thelarche by 13 years of age. Developmental changes during puberty in girls occur over a period of 3 – 5 years, usually between 10 and 15 years of age. They include the occurrence of secondary characteristics beginning with breast development, the adolescent growth spurt, the onset of menarche – which does not correspond to the end of puberty – and the acquisition of fertility, as well as profound psychological modifications.

The normal variation in the age at which adolescent changes occur is so wide that puberty cannot be considered to be pathologically delayed until the menarche has failed to occur by the age of 18 or testicular development by the age of 20.

The sources of the data, and a fuller description of normal timing and sequence of pubertal events, as well as the hormonal changes that drive them, are provided in the principal article on puberty. It is worthwhile to consider the world geographical and ethnographic/demographic limits and deficits of this study.

Women with the condition may be asymptomatic and unaware of having a double uterus. However, a study by Heinonen showed that certain conditions are more common. In his study of 26 women with a double uterus gynecological complaints included dysmenorrhea and dyspareunia. All patients displayed a double vagina. The fetal survival rate in 18 patients who delivered was 67.5%. Premature delivery occurred in 21% of the pregnancies. Breech presentation occurred in 43% of women and cesarean section was performed in 82% of the cases.

A specific association of uterus didelphys (double uterus), unilateral hematocolpos (inadequate draining of menstrual blood) and ipsilateral renal agenesis (having only one kidney) has been described.

An individual with this condition is hormonally normal; that is, the person will enter puberty with development of secondary sexual characteristics including thelarche and adrenarche (pubic hair). The person's chromosome constellation will be 46,XX. At least one ovary is intact, if not both, and ovulation usually occurs. Typically, the vagina is shortened and intercourse may, in some cases, be difficult and painful. Medical examination supported by gynecologic ultrasonography demonstrates a complete or partial absence of the cervix, uterus, and vagina.

If there is no uterus, a person with MRKH cannot carry a pregnancy without intervention. It is possible for the person to have genetic offspring by in vitro fertilization (IVF) and surrogacy. Successful uterine transplant has been performed in limited numbers of patients, resulting in several live births, but the technique is not widespread or accessible to many women.

A person with MRKH typically discovers the condition when, during puberty years, the menstrual cycle does not start (primary amenorrhoea). Some find out earlier through surgeries for other conditions, such as a hernia.

Preterm birth causes a range of problems.

The main categories of causes of preterm birth are preterm labor induction and spontaneous preterm labor. Signs and symptoms of preterm labor include four or more uterine contractions in one hour. In contrast to false labour, true labor is accompanied by cervical dilatation and effacement. Also, vaginal bleeding in the third trimester, heavy pressure in the pelvis, or abdominal or back pain could be indicators that a preterm birth is about to occur. A watery discharge from the vagina may indicate premature rupture of the membranes that surround the baby. While the rupture of the membranes may not be followed by labor, usually delivery is indicated as infection (chorioamnionitis) is a serious threat to both fetus and mother. In some cases, the cervix dilates prematurely without pain or perceived contractions, so that the mother may not have warning signs until very late in the birthing process.

A review into using uterine monitoring at home to detect contractions and possible preterm births in women at higher risk of having a preterm baby found that it did not reduce the number of preterm births. The research included in the review was poor quality but it showed that home monitoring may increase the number of unplanned antenatal visits and may reduce the number of babies admitted to special care when compared with women receiving normal antenatal care.

Preterm infants usually show physical signs of prematurity in reverse proportion to the gestational age. As a result, they are at risk for numerous medical problems affecting different organ systems.

- Neurological problems include apnea of prematurity, hypoxic-ischemic encephalopathy (HIE), retinopathy of prematurity (ROP), developmental disability, transient hyperammonemia of the newborn, cerebral palsy and intraventricular hemorrhage, the latter affecting 25 percent of babies born preterm, usually before 32 weeks of pregnancy. Mild brain bleeds usually leave no or few lasting complications, but severe bleeds often result in brain damage or even death. Neurodevelopmental problems have been linked to lack of maternal thyroid hormones, at a time when their own thyroid is unable to meet postnatal needs.

- Cardiovascular complications may arise from the failure of the ductus arteriosus to close after birth: patent ductus arteriosus (PDA).

- Respiratory problems are common, specifically the respiratory distress syndrome (RDS or IRDS) (previously called hyaline membrane disease). Another problem can be chronic lung disease (previously called bronchopulmonary dysplasia or BPD).

- Gastrointestinal and metabolic issues can arise from neonatal hypoglycemia, feeding difficulties, rickets of prematurity, hypocalcemia, inguinal hernia, and necrotizing enterocolitis (NEC).

- Hematologic complications include anemia of prematurity, thrombocytopenia, and hyperbilirubinemia (jaundice) that can lead to kernicterus.

- Infection, including sepsis, pneumonia, and urinary tract infection

A study of 241 children born between 22 and 25 weeks who were currently of school age found that 46 percent had severe or moderate disabilities such as cerebral palsy, vision or hearing loss and learning problems. 34 percent were mildly disabled and 20 percent had no disabilities, while 12 percent had disabling cerebral palsy.

Hair diseases are disorders primarily associated with the follicles of the hair.

A few examples are

- Alopecia

- Bubble hair deformity

- Hair casts

- Hair loss

- hypertrichosis

- Ingrown hair

- Monilethrix

- Premature greying of hair

- Pattern hair loss

- Trichorrhexis invaginata

Many hair diseases can be associated with distinct underlying disorders.

Piedra are fungal diseases.

Hair disease may refer to excessive shedding or baldness (or both). Balding can be localised or diffuse, scarring or non-scarring. Increased hair can be due to hormonal factors (hirsutism) or non-hormonal (hypertrichosis). Scalp disorders may or may not be associated with hair loss.

Müllerian agenesis or müllerian aplasia, Mayer–Rokitansky–Küster–Hauser syndrome, or vaginal agenesis is a congenital malformation characterized by a failure of the Müllerian duct to develop, resulting in a missing uterus and variable degrees of vaginal hypoplasia of its upper portion. Müllerian agenesis (including absence of the uterus, cervix and/or vagina) is the cause in 15% of cases of primary amenorrhoea. Because most of the vagina does not develop from the Müllerian duct, instead developing from the urogenital sinus along with the bladder and urethra, it is present even when the Müllerian duct is completely absent.

Because ovaries do not develop from the Müllerian ducts, affected women might have normal secondary sexual characteristics but are infertile due to the lack of a functional uterus. However, motherhood is possible through use of gestational surrogates. Mayer-Rokitansky-Küster-Hauser syndrome (MRKH) is hypothesized to be a result of autosomal dominant inheritance with incomplete penetrance and variable expressivity, which contributes to the complexity involved in identifying of the underlying mechanisms causing the condition. Because of the variance in inheritance, penetrance and expressivity patterns, MRKH is subdivided into two types: type 1, in which only the structures developing from the Müllerian duct are affected (the upper vagina, cervix, and uterus), and type 2, where the same structures are affected, but is characterized by the additional malformations of other body systems most often including the renal and skeletal systems. MRKH type 2 includes MURCS (Müllerian Renal Cervical Somite). The majority of MRKH syndrome cases are characterized as sporadic, but familial cases have provided evidence that, at least for some patients, MRKH is an inherited disorder. The underlying causes of MRKH syndrome is still being investigated, but several causative genes have been studied for their possible association with the syndrome. Most of these studies have served to rule-out genes as causative factors in MRKH, but thus far, only WNT4 has been associated with MRKH with hyperandrogenism.

The medical eponym honors August Franz Josef Karl Mayer (1787–1865), Carl Freiherr von Rokitansky (1804–1878), Hermann Küster (1879–1964), and Georges Andre Hauser (1921–2009).

Other things to keep in mind that may present similarly to premature rupture of membranes are the following:

- Urinary incontinence: leakage of small amounts of urine is common in the last part of pregnancy

- Normal vaginal secretions of pregnancy

- Increased sweat or moisture around the perineum

- Increased cervical discharge: this can happen when there is a genital tract infection

- Semen

- Douching

- Vesicovaginal fistula: an abnormal connection between the bladder and the vagina

- Loss of the mucus plug

Like amniotic fluid, blood, semen, vaginal infections, antiseptics, basic urine, and cervical mucus also have a basic pH and can also turn nitrazine paper blue. Cervical mucus can also make a pattern similar to ferning on a microscope slide, but it is usually patchy and with less branching.

The sex steroid consequences of severe 3β-HSD CAH are unique among the congenital adrenal hyperplasias: it is the only form of CAH that can produce ambiguity in both sexes. As with 21-hydroxylase deficient CAH, the degree of severity can determine the magnitude of over- or undervirilization.

In an XX (genetically female) fetus, elevated amounts of DHEA can produce moderate virilization by conversion in the liver to testosterone. Virilization of genetic females is partial, often mild, and rarely raises assignment questions. The issues surrounding corrective surgery of the virilized female genitalia are the same as for moderate 21-hydroxylase deficiency but surgery is rarely considered desirable.

The extent to which mild 3β-HSD CAH can cause early appearance of pubic hair and other aspects of hyperandrogenism in later childhood or adolescence is unsettled. Early reports about 20 years ago suggesting that mild forms of 3β-HSD CAH comprised significant proportions of girls with premature pubic hair or older women with hirsutism have not been confirmed and it now appears that premature pubarche in childhood and hirsutism after adolescence are not common manifestations of 3β-HSD CAH.

Undervirilization of genetic males with 3β-HSD CAH occurs because synthesis of testosterone is impaired in both adrenals and testes. Although DHEA is elevated, it is a weak androgen and too little testosterone is produced in the liver to offset the deficiency of testicular testosterone. The degree of undervirilization is more variable, from mild to severe. Management issues are those of an undervirilized male with normal sensitivity to testosterone.

If the infant boy is only mildly undervirilized, the hypospadias can be surgically repaired, testes brought into the scrotum, and testosterone supplied at puberty.

Management decisions are more difficult for a moderately or severely undervirilized genetic male whose testes are in the abdomen and whose genitalia look at least as much female as male. Male sex can assigned and major reconstructive surgery done to close the midline of the perineum and move the testes into a constructed scrotum. Female sex can be assigned and the testes removed and vagina enlarged surgically. A recently advocated third choice would be to assign either sex and defer surgery to adolescence. Each approach carries its own disadvantages and risks. Children and their families are different enough that none of the courses is appropriate for all.

The mineralocorticoid aspect of severe 3β-HSD CAH is similar to those of 21-hydroxylase deficiency. Like other enzymes involved in early stages of both aldosterone and cortisol synthesis, the severe form of 3β-HSD deficiency can result in life-threatening salt-wasting in early infancy. Salt-wasting is managed acutely with saline and high-dose hydrocortisone, and long-term fludrocortisone.

Young males are most often affected, though similar symptoms have been reported in females with excessive vaginal discharge or leucorrhea, which is also considered a "vital fluid".

Premature ejaculation and impotence are commonly seen. Other somatic symptoms like weakness, easy fatiguability, palpitations, insomnia, low mood, guilt and anxiety are often present. Males sometimes report a subjective feeling that their penises have shortened. These symptoms are usually associated with an anxious and dysphoric mood state.

Some doctors believe dhat syndrome to be either a culture-bound presentation of clinical depression, as a somatized set of symptoms, or a result of Western doctors' misinterpretation of patients' descriptions of their condition.

It is very common in Nepali culture as well. Most of them come with the complaints of "drops" and become extremely anxious about it and see it as loss of "male power". It is often related with obsessive ruminations and somatoform symptoms. Others see it as a distinct clinical entity which is less culture-bound than these critics assert, and describe it as one form of a syndrome of "semen-loss anxiety" which also occurs in other Eastern cultures as jiryan and shen-k'uei, as well as in Western cultures.

Chlamydia infection might also be related to it because of similar symptoms in case of infection of the urethra (urethritis), which is usually symptomatic, causing a white discharge from the penis with or without pain on urinating (dysuria).

Premature ejaculation (PE) occurs when a man experiences orgasm and expels semen soon after sexual activity and with minimal penile stimulation. It has also been called "early ejaculation," "rapid ejaculation," "rapid climax," "premature climax," and (historically) "ejaculatio praecox." There is no uniform cut-off defining "premature", but a consensus of experts at the International Society for Sexual Medicine endorsed a definition including "ejaculation which always or nearly always occurs prior to or within about one minute". The International Classification of Diseases (ICD-10) applies a cut-off of 15 seconds from the beginning of sexual intercourse. Hong argued that rapid ejaculation is an evolutionary adaptation.

Although men with premature ejaculation describe feeling that they have less control over ejaculating, it is not clear if that is true, and many or most average men also report that they wish they could last longer. Men's typical ejaculatory latency is approximately 4–8 minutes. The opposite condition is delayed ejaculation.

Men with PE often report emotional and relationship distress, and some avoid pursuing sexual relationships because of PE-related embarrassment. Compared with men, women consider PE less of a problem, but several studies show that the condition also causes female partners distress.